Heart wall tension reduction apparatus and method

Abstract

Devices and methods for treatment of a failing heart by reducing the heart wall stress. The device can be one which reduces wall stress throughout the cardiac cycle or only a portion of the cardiac cycle.

Description

RELATED APPLICATIONS[0001]This application is a continuation-in-part of U.S. application Ser. No. 09 / 985,361 of Cyril J. SCHWEICH, Jr. et al. for HEART WALL TENSION REDUCTION APPARATUS AND METHOD, filed Nov. 2, 2001 now U.S. Pat. No. 6,589,160, which is a continuation of U.S. application Ser. No. 09 / 697,597, filed Oct. 27, 2000, now U.S. Pat. No. 6,332,864, which is a continuation of application Ser. No. 09 / 492,777, filed Jan. 28, 2000, now U.S. Pat. No. 6,162,168, which is a continuation of application Ser. No. 08 / 778,277, filed Jan. 2, 1997, now U.S. Pat. No. 6,050,936.[0002]This application also is a continuation-in-part of U.S. application Ser. No. 09 / 843,078 of Todd J. MORTIER et al. for STRESS REDUCTION APPARATUS AND METHOD, filed Apr. 27, 2001 now U.S. Pat. No. 6,402,680, which is a continuation of application Ser. No. 09 / 522,068, filed Mar. 9, 2000, now U.S. Pat. No. 6,264,602, which is a continuation of application Ser. No. 09 / 124,321, filed Jul. 29, 1998, now U.S. Pat. No....

AI Technical Summary

Benefits of technology

[0011]The present invention pertains to a non-pharmacological, passive apparatus for the treatment of a failing heart. The device is configured to reduce the tension in the heart wall. It is believed to reverse, stop or slow the disease process of a failing heart as it reduces the energy consumption of the failing heart, decrease in isovolumetric contraction, increases sarcomere shortening during contraction and an increase in isotonic shortening in turn increases stroke volume. In embodiments, the device reduces wall tension during diastole (preload) and systole.

[0014]The present invention also pertains to a device and method for reducing mechanical heart wall muscle stress. Heart muscle stress is a stimulus for the initiation and progressive enlargement of the left ventricle in heart failure. Reduction of heart wall stress with the devices and methods disclosed herein is anticipated to substantially slow, stop or reverse the heart failure disease process. Although the primary focus of the discussion of the devices and methods of the present invention herein relates to heart failure and the left ventricle, these devices and method could be used to reduce stress in the heart's other chambers.

[0015]The devices and methods of the present invention can reduce heart wall stress throughout the cardiac cycle including end diastole and end systole. Alternatively, they can be used to reduce wall stress during the portions of the cardiac cycle not including end systole. Those devices which operate throughout the cardiac cycle are referred to herein as “full cycle splints”. Those devices which do not operate to reduce wall stress during end stage systole are referred to as “restrictive devices”. Restrictive devices include both “restrictive splints” which alter the geometric shape of the left ventricle, and “wraps” which merely limit the magnitude of the expansion of the left ventricle during diastolic filling without a substantial shape change.

[0016]While it is desirable to reduce wall stress for the treatment of heart failure, to slow or reverse the disease process and to increase heart wall muscle shortening and pumping efficiency, it is also desirable to maintain or improve stroke volume and allow for variable preload.

[0018]In asymptomatic, early stage heart failure, it may be possible to use only a restrictive device or method as elevated wall stress is considered to be an initiator of muscle damage and chamber enlargement. Restrictive devices and methods acting during diastole will reduce the maximum wall stress experienced during end diastole and early systole. It should be understood that restrictive devices and methods can be used in combination with full cycle splinting to more precisely control or manipulate stress reduction throughout the cardiac cycle.

Problems solved by technology

With damage to the myocardium or chronic volume overload, however, there are increased requirements put on the contracting myocardium to such a level that this compensated state is never achieved and the heart continues to dilate.

The basic problem with a large dilated left ventricle is that there is a significant increase in wall tension and / or stress both during diastolic filling and during systolic contraction.

However, in a failing heart, the ongoing dilatation is greater than the hypertrophy and the result is a rising wall tension requirement for systolic contraction.

This is felt to be an ongoing insult to the muscle myocyte resulting in further muscle damage.

Additionally, because of the lack of cardiac output, there is generally a rise in ventricular filling pressure from several physiologic mechanisms.

These drug therapies offer some beneficial effects but do not stop the progression of the disease.

Heart transplantation has serious limitations including restricted availability of organs and adverse effects of immunosuppressive therapies required following heart transplantation.

However, this extremely invasive procedure reduces muscle mass of the heart.

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